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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sulpiride (20 mg/kg/ip for 21 days) induced in female rats a significant body weight increase and hyperphagia. After drug withdrawal a significant hypophagia was observed. It is hypothesised that this hypophagia might be a spontaneous manifestation of D2 dopamine receptors supersensitivity, either in the perifornical region of the lateral hypothalamus or in the pituitary.
Med Hypotheses 1989 Sep
PMID:Hypophagia after long-term administration of sulpiride in adult female rats: a model of D2 dopamine receptors supersensitivity? 252 18

1. The effects of starvation post partum (24 h) and tumour growth pre partum on the initiation of lactation in the rat were studied. 2. Tumour growth decreased food intake at 24 h, but not at 2 days post partum. 3. Pup growth rate increased with hyperphagia; starvation and tumour burden decreased pup growth, and starvation decreased maternal body weight. 4. Starvation decreased gastrointestinal-tract mass; tumour growth decreased gastrointestinal-tract and mammary-gland mass. 5. Mammary-gland DNA-synthesis rate was high immediately post partum, but decreased by day 3 of lactation; starvation and tumour burden decreased this rate, and also decreased gastrointestinal-tract DNA-synthesis rate. 6. Arteriovenous differences for glucose and lactate across the mammary gland did not change with time, nor were they affected by the tumour. Starvation decreased arterial glucose and lactate, and the gland extracted less glucose but produced lactate. 7. Mammary-gland lipogenesis was sensitive to starvation and to tumour growth. 8. In contrast with the gradual development of mammary-gland lipogenic enzyme activities, lipoprotein lipase activity was high in the gland by 2 days post partum; starvation or tumour burden decreased the activity. 9. The mammary gland is sensitive post partum to decreased food intake, and to tumour presence. The effects of the latter are apparently independent of hypophagia.
Biochem J 1989 Sep 15
PMID:Lipid metabolism during the initiation of lactation in the rat. The effects of starvation and tumour growth. 259 Jan 73

Despite the obese Zucker rat's hyperphagia on carbohydrate diets such as laboratory chow, this laboratory has found that its satiety response to glucose and other simple sugars is comparable to that of its lean control rat. To further investigate carbohydrate satiety in the Zucker rat, the short-term feeding behavior of obese and lean rats was observed following intragastric infusions (7.2 kcal in 10 ml) of corn starch and the starch hydrolysates Polycose and dextrin. There were no reliable between-genotype differences in the feeding inhibitory effects of Polycose and dextrin. However, in obese rats, the satiety effect of corn starch was delayed and reduced compared to that observed in lean rats (p less than 0.04). To modify the effect of corn starch, rats were administered 0.2 or 0.6 mg/infusion of the carbohydrate digestive inhibitor acarbose (Bay g 5421). Acarbose significantly reduced the satiety effect of corn starch in lean rats (p less than 0.001), and further attenuated satiety in obese rats (p less than 0.02). Since secretion of pancreatic amylase, the enzyme that initiates starch digestion, is decreased in obese rats, this result suggests that alterations of digestive and/or absorptive processes may underlie the obese rat's impaired satiety response to complex carbohydrate.
Physiol Behav 1989 Sep
PMID:Satiety in the obese Zucker rat: effects of carbohydrate type and acarbose (Bay g 5421). 262 81

Sixty patients who met Research Diagnostic Criteria for major, intermittent, or minor depressive disorder and had reactive mood without atypical symptoms were treated with imipramine hydrochloride, phenelzine sulfate, or a placebo. These patients, referred to as simple mood reactive depressives, were contrasted with previously published data from 180 atypical depressives. Atypical depressives had the presence of at least one vegetative atypical sign (hypersomnia, hyperphagia, leaden feeling, or rejection sensitivity) but were otherwise indistinguishable from simple mood reactive depressives. In contrast to the atypical depressives for whom phenelzine was effective and imipramine was relatively ineffective, both medications were equivalently good in simple mood reactive depressives. Since all groups did poorly when given a placebo and well when given phenelzine, the salient feature of atypical symptoms may be that they predict poor response to imipramine. Since the difference between imipramine and placebo depends on the diagnostic group, pharmacologic dissection suggests that atypical symptoms in patients with nonautonomous mood may delineate a qualitatively distinct subgroup.
Arch Gen Psychiatry 1989 Sep
PMID:Phenelzine and imipramine in mood reactive depressives. Further delineation of the syndrome of atypical depression. 267 30

Hyperglycaemic hyperosmolar non-ketotic syndrome (HHNS) is a life-threatening complication of uncontrolled diabetes mellitus. This syndrome is characterised by severe hyperglycaemia, a marked increase in serum osmolality, and clinical evidence of dehydration without significant accumulation of ketoacids. HHNS is typically observed in elderly patients with non-insulin-dependent diabetes mellitus, although it may rarely be a complication in younger patients with insulin-dependent diabetes, or those without diabetes following severe burns, parenteral hyperalimentation, peritoneal dialysis, or haemodialysis. Patients receiving certain drugs including diuretics, corticosteroids, beta-blockers, phenytoin, and diazoxide are at increased risk of developing this syndrome. Patients usually present with a prolonged phase of osmotic diuresis leading to severe depletion of both the intracellular and extracellular fluid volumes. Losses of water exceed those of sodium, resulting in hypertonic dehydration. Therefore, correction of the syndrome will ultimately require administration of hypotonic fluids. Patients presenting with HHNS also have significant depletion of potassium and other electrolytes that will need to be replaced. The principal goal at the outset of therapy must be restoration of the intravascular volume to assure adequate perfusion of vital organs. It remains controversial whether 0.9% or 0.45% NaCl should be the initial fluid infused intravenously. We prefer to administer 0.9% NaCl until the vital signs have stabilised and then substitute 0.45% NaCl. 10 to 15 units of regular human insulin should be injected as a bolus, followed by a continuous infusion of approximately 0.1 U/kg/h. Once the blood glucose approaches 13.9 to 16.7 mmol/L (250 to 300) mg/dl, 5% dextrose should be added to the intravenous fluids and the rate of insulin infusion reduced. Following recovery many patients presenting with HHNS will not require long term insulin therapy and can be managed effectively with diet or oral agents. Precipitating causes of HHNS must be identified and treated simultaneously with correction of the metabolic abnormalities. Appropriate management of precipitating illnesses will limit the high mortality associated with HHNS. This review discusses the current state of knowledge concerning the pathogenesis of HHNS, the clinical features of the disorder, and a systematic approach to treatment.
Drugs 1989 Sep
PMID:Treatment of hyperglycaemic hyperosmolar non-ketotic syndrome. 268 Apr 38

A variety of devices is now available for venous access in patients requiring long-term infusions of chemotherapeutic agents, hyperalimentation solutions, blood products or antibiotics. All have advantages and disadvantages which may make the selection of one type of device appropriate under a given set of circumstances but inappropriate in another. Experience has shown that patients needing intensive therapy for hematologic malignancies are best served by lines that require minimal dissection for insertion, such as the Hickman catheter. Patients who are unlikely to hemorrhage at the time of insertion and who need only intermittent therapy can take advantage of the greater convenience and cosmetic appearance of a totally implantable port. Peripheral vein cannulation by means of fine silicone rubber catheters can be performed by trained intravenous nurses to provide access of intermediate duration without the expense and inconvenience of surgical insertion in an operating room.
Eur J Cancer Clin Oncol 1989 Sep
PMID:Choosing an appropriate implantable device for long-term venous access. 268 May 19

Marked weight loss is the major nutritional defect in chronic pancreatitis. Inadequate food intake owing to recurrent or near continuous pain usually accounts for the initial 10 to 20 per cent of loss of body weight, which decreases again with the onset of diabetes and is often precipitous with the development of steatorrhea. Treatment of pain, control of diabetes, and intensive pancreatic replacement therapy for steatorrhea usually causes weight gain, but seldom to ideal weight. It appears that the patient's body weight gets set at a new "weight-stat." Although isolated abnormalities of small bowel function tests can be elicited and deficiencies of fat-soluble vitamins, calcium, zinc, selenium, and so forth may be demonstrated, these rarely lead to clinical syndromes, as with demonstrable low B12 uptake in some 10 to 15 per cent of patients. In the late stage of the disease and particularly in NATP, extreme protein-calorie malnutrition may occur, which may not be correctable even by hyperalimentation. Although the mortality of the disease was reportedly higher in areas of socioeconomic deprivation, it appears from recent studies in Switzerland and other developed countries that mortality during a 12-year period may be in the region of 50 per cent worldwide.
Gastroenterol Clin North Am 1989 Sep
PMID:Nutritional deficiencies in chronic pancreatitis. 268 Sep 66

The effects of streptozotocin-induced diabetes on weight gain, bone growth and GH secretion have been studied in conscious chronically cannulated male rats. In addition to the classic diabetic symptoms (hyperphagia, polydipsia, polyuria, glycosuria and hyperglycaemia), the slow body weight gain (0.95 +/- 0.5 compared with 2.63 +/- 0.5 g/day in non-diabetic controls) was associated with a reduction in bone growth (from 162 +/- 9 to 48 +/- 4 microns/day) and a reduced pituitary GH content (from 1.5 +/- 0.2 to 0.6 +/- 0.06 mg/gland). Serial blood sampling during the day or overnight showed that the normal male episodic GH secretory pattern was obliterated in the diabetic animals. The constant osmotic stimulation of hyperglycaemia and high fluid turnover was reflected in a significant reduction in pituitary oxytocin and arginine vasopressin (AVP) stores. Intravenous insulin infusions (67-1340 pmol/h for 4 or 7 days) caused a large initial weight gain (greater than 20 g in 2 days) followed by a slower increase, and stimulated tibial bone growth (to 100 +/- 16 and 126 +/- 8 microns/day after 4 or 7 days respectively). Insulin infusion for 7 days also increased pituitary GH content (to 1 +/- 0.15 mg/gland), and the normal episodic GH secretory pattern returned. Intravenous infusions of insulin which reduced, but did not completely normalize, blood glucose levels, allowed the resumption of growth and pulsatile GH secretion. Continuous infusion of recombinant human insulin-like growth factor-I (hIGF-I) at 1110 pmol/h for 54 h also caused a large initial rise in body weight in diabetic rats (17.1 +/- 1.6 compared with 7.5 +/- 2.8 g in saline-infused controls) due primarily to increased fluid retention. This effect of hIGF-I occurred without any significant changes in pituitary GH, AVP, oxytocin, blood glucose or bone growth over this short-term infusion, nor was there any obvious effect on spontaneous GH secretion, monitored over the entire infusion period. We conclude that the diabetic rat is not a good model to study growth stimulation by short-term insulin or IGF-I treatments because the insulin-like effects of these peptides obscure their specific growth-promoting activities in this model.
J Endocrinol 1989 Sep
PMID:Growth hormone and growth in diabetic rats: effects of insulin and insulin-like growth factor-I infusions. 268

Urinary incontinence affects up to 43 per cent of acute care patients. Toileting is a function of intact bladder, sphincters, and nervous system. Five types of incontinence are stress, urge, reflex, total, and functional. Problems affecting patients in acute care are: 1. Diagnostic studies 2. Treatments--for example, intravenous fluids, hyperalimentation, medications, catheters 3. Bedrest 4. Restraints 5. Pain 6. Iatrogenic conditions 7. Environment Assessment includes a specific history and physical examination, focused on previous episodes of incontinence, functional ability, and cognitive status. Management includes scheduled fluid intake and toileting, manipulation of the environment, and attention to orientation and psychological factors. The treatment of fecal incontinence in the hospital elderly includes: 1. Assessment of incontinence and contributing factors; 2. Bowel regimen and environmental assists for persons with periodic incontinence; 3. Treatment of diarrhea or constipation; and 4. Protection of perineal skin from stool exposure.
Nurs Clin North Am 1989 Sep
PMID:Continence issues in acute care. 277 95

Adult rats (12 wk of age) fed a wet, high starch diet consumed more energy, gained more weight, and had more carcass fat than rats fed the same diet in a dry form. In contrast, juvenile rats (3.5 wk of age) did not consume more energy, gain more weight, or become fatter when fed the wet, high starch diet than when fed the same diet in dry form. Although rats of both age groups fed high fat diets consumed more energy than rats fed high starch diets, the effect of the high fat diets was much smaller in juvenile than in adult rats. The level of dietary protein (20 vs. 8%) in the diets did not interact with diet type, but juvenile rats fed low protein diets gained less weight than juvenile rats fed standard protein diets. Additional experiments showed that juvenile rats fed a 20% protein diet were capable of increasing fluid intake and energy intake when given sweetened water or insulin, respectively. Thus, low susceptibility to dietary hyperphagia in juvenile rats cannot be explained by assuming that juvenile rats already eat as much as they can. These data are consistent with the possibility that developmental changes in taste responsiveness may contribute to this effect of age.
J Nutr 1989 Sep
PMID:Resistance to dietary hyperphagia in juvenile rats. 279 47


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